2000
DOI: 10.1002/1096-9926(200012)62:6<420::aid-tera9>3.0.co;2-8
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Nonspecific stimulation of the maternal immune system. II. Effects on gene expression in the fetus

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Cited by 47 publications
(20 citation statements)
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“…Certain cytokines of macrophage origin, interleukin-1b (IL-1b), tumour necrosis factor-a (TNF-a) and interferon are suspected of causing pregnancy loss and miscarriage (Raghupathy 1997). Transforming growth factor-b 2 (TGF-b 2 ) and TNF-a have been suggested as having a regulatory function in gene expression during organogenesis (Sharova et al 2000). Furthermore, a study to evaluate the possible involvement of a cytokine involved in pregnancy loss indicated that granulocytemacrophage colony-stimulating factor mediates the early stages of pregnancy loss via modulation of TNF-a and TGF-b 2 activity (Savion et al 2002).…”
mentioning
confidence: 99%
“…Certain cytokines of macrophage origin, interleukin-1b (IL-1b), tumour necrosis factor-a (TNF-a) and interferon are suspected of causing pregnancy loss and miscarriage (Raghupathy 1997). Transforming growth factor-b 2 (TGF-b 2 ) and TNF-a have been suggested as having a regulatory function in gene expression during organogenesis (Sharova et al 2000). Furthermore, a study to evaluate the possible involvement of a cytokine involved in pregnancy loss indicated that granulocytemacrophage colony-stimulating factor mediates the early stages of pregnancy loss via modulation of TNF-a and TGF-b 2 activity (Savion et al 2002).…”
mentioning
confidence: 99%
“…Although the matter of how immune substrates and teratogenic metabolites interact at the cellular level is not yet clear, it is currently proposed that maternal immune stimulation may reduce chemically induced morphological lesions by an indirect effect via regulatory cytokine product of activated immune cells, in this respect Sharova et al (2000) theorized that such soluble mediators restore the teratogen-altered expression of critical fetal genes.…”
Section: Discussionmentioning
confidence: 99%
“…This phenomenon can be explained by lack of morphological signs of cartilage and other joint structure destruction, unvascularisation of epiphyses and immaturity of fetal immune system. High TNF-α expression is a consequence of the fact that this proinflammatory cytokine is one of the indispensable factor in organo-and fetogenesis (Sharova et al, 2000). Its expression argues a high developmental dynamic in the examined epiphyses.…”
Section: Control C3mentioning
confidence: 99%